Delayed Cerebral Energy Failure After Acute Hypoxia-Ischemia in Neworn Piglet Under 48hours of Continuous Monitoring Using Near-Infrared Spectroscopy.
- Author:
Yun Sil CHANG
1
;
Won Soon PARK
;
Munhyang LEE
;
Ki Soo KIM
;
Son Moon SHIN
;
Jung Hwan CHOI
Author Information
1. Department of Pediatrics, Samsung Medical Center, Sung Kyun Kwan University College of Medicine
- Publication Type:Original Article
- Keywords:
Perinatal asphyxia;
Newborn;
Animal;
Near infrared spectroscopy;
Hypoxia;
Ischemia
- MeSH:
Adenosine Triphosphatases;
Adenosine Triphosphate;
Animals;
Anoxia;
Brain;
Carotid Artery, Common;
Glucose;
Heart Rate;
Hemodynamics;
Humans;
Hydrogen-Ion Concentration;
Infant, Newborn;
Critical Care;
Ischemia;
Lactic Acid;
Models, Animal;
Oxygen;
Phosphocreatine;
Polymerase Chain Reaction;
Reperfusion;
Respiration;
Resuscitation;
Spectroscopy, Near-Infrared*;
Spectrum Analysis
- From:Journal of the Korean Pediatric Society
1998;41(9):1198-1209
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To test the hemodynamic and biochemical sequences of secondary cerebral energy failure after acute reversed hypoxic ischemic brain insult (HI) can be reproduced in newborn piglets. METHODS: Fifteen anesthetized, ventilated newborn piglet (<3 day) were studied. Eight (HI) were induced transient HI by breathing 8% oxygen and complete occlusion of bilateral common carotid arteries for 30 minutes followed by reoxygenation and reperfusion. Seven (control) were given a sham operation. Both groups were maintained for 48 hours with intensive care and monitoring of cerbral hemodynamics and [delta Cyt aa3] using near infrared spectroscopy (NIRS). Finally, brain cortex was harvested and determined activities of Na+, K+/-ATPase, level of conjugated dienes, ATP and phosphocreatine (PCr) biochemically. RESULTS: No changes took place in the 48-hour control group. In HI group, PaO2, pH, and MABP decreased, and heart rate, glucose, lactate level in blood and lactate level in CSF increased during acute HI. These variables subsequently returned to normal with time. In continuous NIRS monitoring, [delta Cyt aa3] were not changed in the control group. But in HI group [delta Cyt aa3] decreased significantly in acute HI and then normalized with resuscitation but gradually decreased and was significantly lower than control group at 48 hours. Cerebral Na+, K+/- ATPase activity and ATP, PCr level of experimental group significantly decreased compared to control group. Cerebral level of conjugated dienes were not significantly different between both group. CONCLUSION: We successfully reproduced secondary cerebral energy failure after acute HI in thenewborn piglet and this animal model may be useful for testing cerebroprotective strategies.
